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Am J Gastroenterol. 1995 Dec;90(12):2134-9.

Clinical assessment of hyperlipidemic pancreatitis.

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Department of Medicine, Medical College of Georgia, Augusta, USA.



This study addresses three questions: 1) What are the clinical presentations of pancreatitis secondary to hyperlipidemia? 2) What is the role of alcohol, diabetes, or known causes of hypertriglyceridemia? and 3) Does the course of pancreatitis secondary to hypertriglyceridemia differ from that of other etiologies?


We reviewed patients between 1982 and 1994 with a diagnosis of pancreatitis (577.0) and hypertriglyceridemia (272.0). Four hospitals participated. Seventy patients had a clinical presentation consistent with pancreatitis, that is elevated amylase and lipase or evidence of pancreatitis by ultrasound or CT imaging and serum triglyceride levels greater than 500 mg/dl or lactescent serum. Clinical data were derived from hospital admissions.


Hypertriglyceridemia was the etiology in 1.3-3.8% of patients discharged with a diagnosis of pancreatitis. A history of diabetes mellitus was present in 72%, hypertriglyceridemia in 77%, alcohol use 23%, and gallstones in 7%. Lipemic serum was described on admission in 45%. Mean triglyceride levels were 4587 +/- 3616 ml/dl. Amylase was elevated two times normal in 54%, and lipase was elevated two times normal in 67%. CT scans were abnormal in 82%, with peripancreatic fluid in 34%, pseudocyst 37%, and necrosis in 15%. Abscess occurred in 13%, death in 6%.


Acute pancreatitis secondary to hyperlipidemia is characterized by three presentations. All patients present with abdominal pain, nausea, and vomiting of hours to days duration. The most common presentation is a poorly controlled diabetic with a history of hypertriglyceridemia. The second presentation is the alcoholic found to have hypertriglyceridemia or lactescent serum on admission. The third, about 15-20% of patients, is the nondiabetic, nonalcoholic, nonobese patient with drug- or diet-induced hypertriglyceridemia.

[Indexed for MEDLINE]

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